Evidence against an increase in capillary permeability in subjects exposed to high altitude
Kleger, Gian-Reto, Peter Bärtsch, Peter Vock, Bernhard Heilig, L. Jackson Roberts II, and Peter E. Ballmer. Evidence against an increase in capillary permeability in subjects exposed to high altitude. J. Appl. Physiol.81(5): 1917-1923, 1996.—A potential pathogenetic cofactor for the development of...
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| Main Authors: | , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
1 November 1996
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| In: |
Journal of applied physiology
Year: 1996, Volume: 81, Issue: 5, Pages: 1917-1923 |
| ISSN: | 1522-1601 |
| DOI: | 10.1152/jappl.1996.81.5.1917 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1152/jappl.1996.81.5.1917 Verlag, lizenzpflichtig, Volltext: https://journals.physiology.org/doi/full/10.1152/jappl.1996.81.5.1917 
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| Author Notes: | Gian-Reto Kleger, Peter Bärtsch, Peter Vock, Bernhard Heilig, L. Jackson Roberts, Peter E. Ballmer |
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| 520 | |a Kleger, Gian-Reto, Peter Bärtsch, Peter Vock, Bernhard Heilig, L. Jackson Roberts II, and Peter E. Ballmer. Evidence against an increase in capillary permeability in subjects exposed to high altitude. J. Appl. Physiol.81(5): 1917-1923, 1996.—A potential pathogenetic cofactor for the development of acute mountain sickness and high-altitude pulmonary edema is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free radical-mediated injury to the lung. We measured the systemic albumin escape by intravenously injecting 5 μCi of125I-labeled albumin and the plasma concentrations of cytokines, F2-isoprostanes (products of lipid peroxidation), and acute-phase proteins in 24 subjects exposed to 4,559 m. Ten subjects developed acute mountain sickness, and four subjects developed high-altitude pulmonary edema. The transcapillary escape rate of albumin was 6.9 ± 2.0%/h (SD) at low (550 m) and 6.3 ± 1.9%/h at high (4,559 m) altitude (P= 0.23; n = 24). The subjects with high-altitude pulmonary edema had a modest but insignificant increase in the transcapillary escape rate of albumin (4.6 ± 1.9%/h at low vs. 5.7 ± 1.9%/h at high altitude;P = 0.42;n = 4). Plasma concentrations of fibrinogen, α1-acid glycoprotein, C-reactive protein, and interleukin-6 were unchanged in the early phases and significantly increased by the end of the observation period in the subjects with high-altitude pulmonary edema, whereas tumor necrosis factor-α and F2-isoprostanes did not change at all. This suggests that the inflammatory reaction was rather a consequence than a causative factor of high-altitude pulmonary edema. In summary, these data argue against a dominant role for increased systemic capillary permeability in the development of acute mountain sickness and high-altitude pulmonary edema. | ||
| 650 | 4 | |a acute mountain sickness | |
| 650 | 4 | |a F2-isoprostanes | |
| 650 | 4 | |a free radicals | |
| 650 | 4 | |a high-altitude pulmonary edema | |
| 650 | 4 | |a vascular permeability | |
| 700 | 1 | |a Bärtsch, Peter |e VerfasserIn |0 (DE-588)1068984023 |0 (DE-627)821117483 |0 (DE-576)428341179 |4 aut | |
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| 700 | 1 | |a Heilig, Bernhard |e VerfasserIn |0 (DE-588)1211351513 |0 (DE-627)1699093865 |4 aut | |
| 700 | 1 | |a Roberts, L. Jackson |e VerfasserIn |4 aut | |
| 700 | 1 | |a Ballmer, Peter E. |e VerfasserIn |4 aut | |
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